1. Field of Invention
The present invention relates to a method of preventing darkening of the skin and a method of inhibiting pigmentation, more particularly relates to a method of preventing darkening of the skin and a method of inhibiting pigmentation by preventing melanization of melanin monomers due to ultraviolet rays.
The present invention also relates to a polymerization inhibitor for inhibiting the polymerization of biological dihydroxyindole due to long wavelength ultraviolet rays (UVA) by 3-O-ethyl ascorbic acid and an external skin treatment composition containing the same.
2. Description of the Related Art
In the past, darkening of the skin caused by ultraviolet rays was explained due to the higher activity of the enzyme tyrosinase in the melanocytes present in the basal layer of epidermis, the increase in the melanin produced from the tyrosine in the melanocytes, and the surrounding keratinocytes receiving the melanin. Therefore, as the method for preventing darkening of the skin caused by ultraviolet rays, kojic acid or arbutin etc. i.e., so-called whitening agents which inhibit the activity or synthesis of tyrosine in addition to ultraviolet ray blockers absorbing or scattering ultraviolet rays are used in the past.
The above process involves the production and synthesis of tyrosinase protein, and therefore it takes at least several days for the increase in the activity of tyrosinase and takes three to five days or so, until the surrounding keratinocytes receive the melanin and the skin appears dark.
However, since the darkening phenomenon caused by excessive exposure to the rays of the sun in leisure activities or while in the ocean occurs within a short time of one day, the present inventors believed that there was a mechanism of action different from the conventionally believed melanin production due to an enzymatic reaction involving tyrosine.
Therefore, we engaged in studies using a solar simulator with the aim of experimentally reproducing the darkening of skin occurring in one day. We divided the ultraviolet rays, which we are routinely exposed to, into medium wavelength ultraviolet rays (UVB: 280 to 320 nm) and long wavelength ultraviolet rays (UVA: 320 to 400 nm) and irradiated the forearms of human subjects with UVB or UVA to examine the changes in darkening over time. As a result, with irradiation by 300 mJ/cm2 of UVB, the skin turned red within one day of the irradiation. This reddening continued for several days, then the skin gradually turned dark from 5 days. This darkness reached a peak on 7 days, and then gradually faded. On the other hand, with irradiation of 5 to 15 J/cm2 of UVA, the skin turned dark immediately after irradiation, that is, immediate darkening occurred. This darkening faded after 3 hours. With irradiation of 16 to 45 J/cm2, however, immediate darkening occurred after the end of the irradiation and this darkness lasted for over a week.
As a result of biochemical and histochemical investigation of the sustained darkening phenomenon due to UVA, we found that melanin is produced due to the relatively stable colorless, melanin monomers such as transparent compound dihydroxyindole carboxylic acid or its related compounds, by the melanocytes present in the base layer of the epidermis directly struck by the UVA.